2.1. Lupus
SLE is a serious autoimmune condition in which abnormal humoral and cellular immune responses occur. This immune complex disorder manifests symptoms such as erosive inflammation of skin (producing a characteristic rash), blood vessel lesions, pleurisy, psychiatric disturbances, convulsions, and inflammation of the kidney glomeruli (leading to renal disfunction or failure). Although various factors have been attributed to the onset of SLE, the precise etiology is not known. It is known that significant concentrations of both gamma-globulin and complement are present in the tissues and such immune complexes are considered the causative agents for the systemic cellular damage which is observed. A wide range of auto-antibodies have been detected in SLE patients including circulating antibodies to lymphocytes, red blood cells, platelets and neutrophils and recognition occurs by all four subclasses of immunoglobulin to cellular components such as nuclei, ribosomes, mitochondria and lysosomes.
The sites of lupus antibody interaction with subcellular components include nucleoproteins, histones and nucleic acids. In the case of nucleic acids, one antigenic determinent appears to be the carbohydrate-phosphate unit.